Current Environmental Health Reports最新文献

Purpose of review: Zinc is an essential micronutrient with a myriad of key roles in human health. This review summarizes mechanistic data supporting the protective effects of zinc on metal toxicity and discusses the framework for an interventional clinical trial of zinc supplementation within a metal exposed Native American community.

Recent findings: Many metals have common underlying mechanisms of toxicity that contribute to adverse human health effects. Studies demonstrate that multiple aspects of metal toxicity can be attributed to disruption of essential zinc-dependent functions. Multiple lines of evidence suggest that zinc may confer protection against metal toxicity in human populations with mixed-metal exposures. Thinking Zinc is a mechanism-informed intervention study of zinc supplementation to test the potential benefits of zinc while maintaining a culturally responsive research approach. The current knowledge of diverse metal and zinc interactions, coupled with strong mechanistic evidence for zinc benefits in the context of toxic metal exposures, supports the hypothesis that zinc supplementation may mitigate the impact of toxic metals exposures in populations with chronic mixed metal exposures and in populations with low zinc status.

Purpose of review: Indoor air pollution is likely to be elevated in multi-family housing and to contribute to health disparities, but limited studies to date have systematically considered the empirical evidence for exposure differentials between multi-family and single-family housing. Our goal is to separately examine the drivers of residential indoor air pollution, including outdoor air pollution, ventilation and filtration, indoor sources, and occupant activity patterns, using secondhand smoke as a case study to examine the behavioral dimensions of indoor environmental interventions.

Recent findings: Within studies published from 2018 to 2023, multi-family homes have higher average outdoor air pollution than single-family homes given their more frequent presence in urban and near-roadway settings. Systematic differences in ventilation were principally related to the presence of working kitchen and bathroom exhaust fans, with heterogeneity in overall building infiltration. Indoor sources such as smoking and cooking were more prevalent in multi-family housing, partly because of the influence of adjacent units and shared spaces and partly because source utilization was higher among sociodemographic groups who tend to live in multi-family housing. The literature on smoke-free housing demonstrated that additional steps would be required to reduce exposure to secondhand smoke given some of the challenges associated with smoking cessation. Publications on the drivers of indoor air pollution in multi-family housing reinforce the likelihood of substantial exposure disparities, indicating the urgency of policy measures that address indoor sources and improve ventilation and filtration in a manner that recognizes the complex behavioral dynamics in the home environment.

Purpose of review: Metals are common environmental pollutants. Acute and chronic exposures to non-essential toxic metals or excessive essential metals cause various diseases including cancer in humans. However, the underlying mechanisms have not been well understood. Long non-coding RNAs (lncRNAs) refer to RNA transcripts that have more than 200 nucleotides but do not have significant protein coding capacities. While lncRNAs were once considered transcription noise, they have become increasingly recognized as crucial players in various physiological and pathogenesis processes. The goal of this article is to review and discuss recent studies that show important roles of lncRNA dysregulations in metal toxicity and carcinogenesis.

Recent findings: Recent studies showed that metal exposures dysregulate expression of lncRNAs in cultured cells, animals and humas. However, only a few studies determined the mechanisms of how metal exposure dysregulated expression of lncRNAs. The majority of the studies reported the association of abnormally expressed lncRNAs with various toxic effects of metal exposures, only limited studies established causal relationships demonstrating causal roles of dysregulated lncRNAs in metal toxicity and carcinogenesis. Mechanistically, most studies reported that dysregulated lncRNAs functioned as microRNA sponges to regulate gene expression, much less studies explored other mechanisms of lncRNA actions. It is evident that metal exposures dysregulate expression of lncRNAs, which may serve as novel mediators in metal toxicity and carcinogenesis. Further studies are needed to establish dysregulated lncRNAs as potential diagnostic biomarkers and therapeutic targets for metal exposure-associated diseases.

Purpose of review: Parking is a ubiquitous feature of the built environment, but its implications for public health are under-examined. This narrative review synthesizes literature to describe pathways through which parking may affect population health.

Recent findings: We begin by contextualizing the issue, outlining key terminology, the sheer scale of land dedicated to parking, and the historical factors that led to this dominant land use. Next, we delineate four pathways linking parking with public health: 1) Promoting driving and car dependency, affecting air pollution, greenhouse-gas emissions, physical activity, traffic-related injuries and fatalities, and accessibility; 2) Creating impervious surfaces, with consequences for urban heat, flooding, water pollution, and green space; 3) Affecting housing affordability and associated health outcomes of this social determinant; and 4) Design, construction, and maintenance, the health impacts of which include on-street parking's positive and negative impacts on safety for all roadway users, air-quality effects of parking's construction and maintenance, and the potential for green parking lots to mitigate some health consequences of impervious surfaces. While evidence supports each pathway, additional empirical research is needed to evaluate impacts of parking on public-health outcomes. As a dominant feature of the built environment with many health implications, parking warrants attention by public-health research and practice.

Purpose of the review: Seizures and epilepsy can be debilitating neurological conditions and have few known causes. Emerging evidence has highlighted the potential contribution of environmental exposures to the etiology of these conditions, possibly manifesting via neuroinflammation and increased oxidative stress in the brain. We conducted a scoping review of epidemiological literature linking air pollution and temperature exposures with incidence and acute aggravation of seizures and epilepsy. We systematically searched PubMed, Embase, Web of Science, and APA PsycINFO databases for peer-reviewed journal articles published in English from inception to February 7, 2024.

Recent findings: We identified a total of 34 studies: 16 examined air pollution exposure, 12 ambient temperature, and six examined both air pollution and ambient temperature. Most studies were conducted in Asia (China, Taiwan, South Korea, and Japan). Nearly all studies retrospectively derived acute (daily average), ambient, and postnatal exposure estimates from ground monitoring systems and ascertained epilepsy cases or seizure events through record linkage with medical records, health registry systems, or insurance claims data. Commonly assessed exposures were particulate matter (PM_2.5, PM₁₀), nitrogen dioxide (NO₂), sulfur dioxide (SO₂), carbon monoxide (CO), ozone (O₃), and daily mean ambient temperature. Overall, the main findings across studies lacked consistency, with mixed results reported for the associations of air pollutants and temperature metrics with both seizure incidence and acute aggravations of epilepsy.

Purpose of review: With only 12% of the human population living in cities meeting the air quality standards set by the WHO guidelines, there is a critical need for coordinated strategies to meet the requirements of a healthy society. One pivotal mechanism for addressing societal expectations on air pollution and human health is to employ strategic modeling within the urban planning process. This review synthesizes research to inform coordinated strategies for a healthy society. Through strategic modeling in urban planning, we seek to uncover integrated solutions that mitigate air pollution, enhance public health, and create sustainable urban environments.

Recent findings: Successful urban planning can help reduce air pollution by optimizing city design with regard to transportation systems. As one specific example, ventilation corridors i.e. aim to introduce natural wind into urban areas to improve thermal comfort and air quality, and they can be effective if well-designed and managed. However, physical barriers such as sound walls and vegetation must be carefully selected following design criteria with significant trade-offs that must be modeled quantitatively. These tradeoffs often involve balancing effectiveness, cost, aesthetics, and environmental impact. For instance, sound walls are highly effective at reducing noise, provide immediate impact, and are long-lasting. However, they are expensive to construct, visually unappealing, and may block views and sunlight. To address the costly issue of sound walls, a potential solution is implementing vegetation with a high leaf area index or leaf area density. This alternative is also an effective method for air pollution reduction with varying land-use potential. Ultimately, emission regulations are a key aspect of all such considerations. Given the broad range of developments, concerns, and considerations spanning city management, ventilation corridors, physical barriers, and transportation planning, this review aims to summarize the effect of a range of urban planning methods on air pollution considerations.

Purpose of review: Hexavalent chromium [Cr(VI)] is a well-established human carcinogen, yet the mechanisms by which it leads to carcinogenic outcomes is still unclear. As a driving factor in its carcinogenic mechanism, Cr(VI) causes DNA double strand breaks and break-repair deficiency, leading to the development of chromosome instability. Therefore, the aim of this review is to discuss studies assessing Cr(VI)-induced DNA double strand breaks, chromosome damage and instability, and neoplastic transformation including cell culture, experimental animal, human pathology and epidemiology studies.

Recent findings: Recent findings confirm Cr(VI) induces DNA double strand breaks, chromosome instability and neoplastic transformation in exposed cells, animals and humans, emphasizing these outcomes as key steps in the mechanism of Cr(VI) carcinogenesis. Moreover, recent findings suggest chromosome instability is a key phenotype in Cr(VI)-neoplastically transformed clones and is an inheritable and persistent phenotype in exposed cells, once more suggesting chromosome instability as central in the carcinogenic mechanism. Although limited, some studies have demonstrated DNA damage and epigenetic modulation are also key outcomes in biopsies from chromate workers that developed lung cancer. Additionally, we also summarized new studies showing Cr(VI) causes genotoxic and clastogenic effects in cells from wildlife, such as sea turtles, whales, and alligators. Overall, across the literature, it is clear that Cr(VI) causes neoplastic transformation and lung cancer. Many studies measured Cr(VI)-induced increases in DNA double strand breaks, the most lethal type of breaks clearly showing that Cr(VI) is genotoxic. Unrepaired or inaccurately repaired breaks lead to the development of chromosome instability, which is a common phenotype in Cr(VI) exposed cells, animals, and humans. Indeed, many studies show Cr(VI) induces both structural and numerical chromosome instability. Overall, the large body of literature strongly supports the conclusion that Cr(VI) causes DNA double strand breaks, inhibits DNA repair and chromosome instability, which are key to the development of Cr(VI)-induced cell transformation.

Purpose of review: Informing the public about environmental risks to health is crucial for raising awareness around hazards, and promoting actions that minimize exposures. Geographic visualizations-geovisualizations-have become an increasingly common way to disseminate web-based information about environmental hazards, displaying spatial variations in exposures and health outcomes using a map. Unfortunately, ineffective geovisualizations can result in inaccurate inferences about a hazard, leading to misguided actions or policies. In this narrative review, we discuss key considerations for the use of geovisualizations to promote environmental health literacy.

Recent findings: Many conventional geovisualizations used for hazard education and risk communication fail to consider how people process visual information. Design choices that prompt viewers to think and feel, leveraging processes such as individual attention, memory, and emotion, could promote improved comprehension and decision making around environmental health risks using geovisualizations. Based on the studies reviewed, we recommend six strategies for designing effective, evidence-based geovisualizations, synthesizing evidence from the cognitive sciences, cartography, and environmental health. These strategies include: Displaying only key data, tailoring and testing geovisualizations with the desired audience, using salient cues, leveraging emotion, aiding pattern recognition, and limiting visual distractions. Geovisualizations offer a promising avenue for advancing public awareness and fostering proactive measures in addressing complex environmental health challenges. This review highlights how incorporating evidence-based design principles into geovisualizations could promote environmental health literacy. More experimental research evaluating geovisualizations, using interdisciplinary approaches, is needed.

Purpose of review: Exposure to toxic metals/metalloids, such as arsenic (As), cadmium (Cd), and lead (Pb), through food consumption is a global public health concern. This review examines the contamination status of these metals/metalloids in food, assesses dietary intake across different populations, and proposes strategies to reduce metal/metalloid exposures throughout the food chain.

Recent findings: For the general population, dietary intake of metals/metalloids is generally lower than health-based guidance values. However, for vulnerable populations, such as infants, children, and pregnant women, their dietary intake levels are close to or even higher than the guidance values. Among different food categories, seafood shows higher total As, but largely present as organic species. Rice accumulates higher As concentration than other cereals, with inorganic As (iAs) and dimethylarsinic acid (DMA) being the main As species. Methylated thioarsenate species, such as dimethylmonothioarsenate, have also been detected in rice. The distribution of iAs and DMA in rice shows geographical variation. Additionally, seafood and cocoa products generally contain more Cd than other food, but seafood consumption does not significantly increase in adverse health effects due to its high zinc and iron content. Compared to As and Cd, Pb concentrations in food are generally lower. To minimize the health risks of metal/metalloid exposure, several strategies are proposed. Food contamination with toxic metals/metalloids poses significant concerns for human health, particularly for vulnerable populations. This review provides scientific evidence and suggestions for policy makers to reduce human exposure of metals/metalloids via dietary intake.